Nandrolone Decanoate associated with exercise training inhibit vascular endothelial growth factor (VEGF) mRNA expression in rat soleus muscle

Androgenic-anabolic steroids (AAS) have been used for both performance improvement and aesthetic reasons. It is well know that high doses of AAS induce serious adverse effects such as skeletal muscle injuries, including increase in the rate of muscle strains/ruptures. Vascular endothelial growth factor (VEGF) is a key factor in angiogenesis induction on both physiological and pathological conditions The aim of this study was to investigate VEGF mRNA expression in rat soleus muscle after jumping training associated with AAS administration. Wistar rats were grouped into: sedentary (S); trained without AAS (T); sedentary nandrolone decanoate (ND)-treated (AAS); and trained with AAS (AAST). The trained groups carried out jumps in water at 32°C.: 4 series of 10 jumps each, with a 30-second interval among series, for 7 weeks, with 50-80% overload of the animal corporal mass. The AAS (Decadurabolin® - 5mg/kg) was injected subcutaneously in the animal’s back twice a week. Real-time PCR analyses showed that training significantly increased VEGF mRNA expression in comparison with the S and AAS groups. When exercise training was associated with nandrolone decanoate, the VEGF mRNA expression was inhibited compared with T group. The inhibition of VEGF expression by AAS administration can decrease angiogenesis in skeletal muscle. These results suggest that the AAS may be strongly prejudicial to muscle remodeling and performance

Role of resistance training in bone macro and micro damages in an estrogen absence animal model

AIMS: We evaluated the effects of resistance training (RT) on bone properties, morphology, and bone extracellular matrix (ECM) remodeling markers in an ovariectomy (OVX) rat model. MAIN METHODS: Thirty-six female rats were divided into four groups: sham sedentary, OVX sedentary, sham RT, and OVX RT. Rats performed RT for ten weeks, during which they climbed a ladder with progressive loads attached to the tail. Tibias were stored for dual-energy X-ray densitometry (DXA), micro-computed tomography (micro-CT), and biomechanical, biophysical, and biochemical analysis. Femurs were stored for morphological, gene expression, and gelatin zymography analysis. KEY FINDINGS: OVX decreased bone mineral density, stiffness, maximal load, and calcium content, which was reversed by RT. The trabecular number, connectivity, and MMP-13 gene expression decreased in OVX groups. Furthermore, OVX increased run-related transcription factor-2 (RUNX-2) and osteoprotegerin (OPG) gene expression, and increased the number of adipocytes in bone marrow and MMP-2 activity. SIGNIFICANCE: RT was efficient in preventing or reversing changes in bone biomechanical properties in OVX groups, improving fracture load and resilience, which is relevant to prevent fractures. On the other hand, RT did not decrease the number of bone adipocytes in the OVX-RT group. However, RT was efficient for increasing trabecular thickness and cortical bone volume, which improved bone resistance. Our findings provide further insights into the mechanisms involved in the role of RT in OVX damage protection